PURPOSE:To describe the histopathologic findings and relevant clinical details of 3 patients undergoing penetrating keratoplasty (PK) after failure of posterior lamellar endothelial keratoplasty (EK). METHODS:Retrospective clinicopathologic case series. Patients 1 and 2 underwent EK for pseudophakic bullous keratopathy. Patient 3 underwent EK for persistent corneal edema secondary to a Descemet membrane (DM) detachment after cataract extraction. Patient 1 had persistent diffuse corneal edema and broad, long-standing iridocorneal adhesions that precluded repeat EK. Patient 2 had high intraocular pressure and severe anterior chamber inflammation 1 day postoperatively with subsequent noncorneal clearing and elected PK over repeat EK. Progressive corneal edema with resultant poor visual acuity after EK was the reason for PK in patient 3. RESULTS:Histopathologic examination disclosed thickened, edematous corneas with attenuated endothelium consistent with graft failure caused by endothelial decompensation in all 3 cases. Although various degrees of posterior lamellar graft detachment were observed in each instance, significant parts of each graft remained adherent to the host stroma or to segments of residual host DM. The wounds in the adherent areas, although discernible, were relatively inconspicuous, resembling those seen at the flap-stromal interface after laser in situ keratomileusis. The donor graft endothelium was atrophic in all cases, and a delicate retrocorneal fibrous membrane was present in 2 cases. Most of the graft in cases 1 and 2 remained adherent, with small areas of peripheral detachment. In contrast, the graft in case 3 adhered peripherally but had separated from the stroma centrally, forming a thin cleft. CONCLUSIONS:Histopathology suggests endothelial decompensation, incomplete graft adherence, and the formation of retrocorneal fibrous membranes as possible etiologies for EK failure. The adherence of endothelial grafts to residual host DM suggests that it may not be necessary to remove optically clear DM before endothelial graft placement. The inconspicuous nature of the EK interface suggests that it may not play a large role in image degradation, although more study is needed.

译文

目的:描述3例后板状内皮细胞成形术(EK)失败后进行穿透性角膜成形术(PK)的患者的组织病理学发现和相关临床细节。
方法:回顾性临床病理病例系列。患者1和2因假晶状体大疱性角膜病变而接受EK。患者3在白内障摘除后因Descemet膜(DM)脱离继发了持续性角膜水肿的EK。患者1具有持续的弥漫性角膜水肿和广泛的,长期存在的虹膜角膜粘连,因此无法进行重复EK。病人2术后1天有高眼压和严重的前房炎症,随后发生非角膜清除,并选择PK超过重复EK。 EK后进行性角膜水肿导致视力较差是3号患者PK的原因。
结果:所有3例患者的病理组织学检查均显示增厚的水肿性角膜伴内皮减弱,这与内皮失代偿引起的移植失败有关。尽管在每种情况下均观察到不同程度的后板状移植物分离,但每个移植物的重要部分仍粘附于宿主基质或残余宿主DM的节段。粘附区域的伤口虽然可以辨认,但是相对不明显,类似于在激光原位角膜磨镶术后在皮瓣-基质界面看到的伤口。在所有情况下,供体移植物内皮均萎缩,2例存在脆弱的角膜后纤维膜。在案例1和案例2中,大多数移植物保持粘附性,周围脱离区域很小。相反,情况3中的移植物在外周粘附,但在中心与基质分开,形成薄裂口。
结论:组织病理学提示内皮功能失代偿,移植物粘附不完全以及角膜后纤维膜的形成可能是导致EK失败的原因。内皮移植物对残余宿主DM的粘附表明,在放置内皮移植物之前,可能没有必要去除光学透明的DM。 EK接口的不起眼的性质表明,尽管需要进行更多研究,但它在图像质量下降中可能不会发挥重要作用。

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